Taurine has antihypertensive and anxiolytic effects.
Jpn J Pharmacol. 1978 Apr;28(2):259-68.
A modulating role of taurine on release of acetylcholine and norepinephrine from neuronal tissues.
Muramatsu M, Kakita K, Nakagawa K, Kuriyama K.
Effects of taurine (2-aminoethanesulfonic acid) on the uptake and release of 14C-acetylcholine (14C-ACh) and 3H-norepinephrine (3H-NE) in the superior cervical ganglion and cerebral cortex of the rat were studied. Taurine suppressed high potassium evoked release of 14C-ACh and 3H-NE from the rat superior cervical ganglia and cerebral cortical slices, while the drug did not modify per se the uptake and unstimulated (spontaneous) release of 14C-ACh and 3H-NE in these tissues. Furthermore, taurine inhibited the release of 3H-NE from the crude synaptosomal (P2) fraction of the rat brain without affecting the uptake. These results suggest that taurine may act as a modulator of neuronal activity, possibly by stabilizing excitable membrane and by suppressing the release of neurotansmitter at synapses.
PMID: 691871 [PubMed - indexed for MEDLINE]
Neuroscience. 1984 Nov;13(3):663-6.
Modulation of noradrenaline uptake and release by taurine in rat cerebral slices.
Kontro P, Korpi ER, Oja OS, Oja SS.
The effects of taurine on the uptake and release of noradrenaline were studied in forebrain slices from control rats and from rats treated with a taurine-free diet supplemented with 2-guanidinoethanesulphonate. Exogenous taurine slightly increased noradrenaline uptake in slices from untreated rats. There were no significant effects by exogenous taurine on spontaneous efflux of noradrenaline. The potassium-stimulated noradrenaline release was enhanced by taurine from frontal cortical slices and suppressed from occipital slices but only in the diet group, in which the endogenous brain taurine concentration had been lowered to one-half of the control concentration. It is suggested that taurine may act via presynaptic alpha-adrenoceptors and/or modify the availability of calcium for the stimulus-secretion coupling process.
PMID: 6527772 [PubMed - indexed for MEDLINE
Adv Exp Med Biol. 1996;403:257-62.
Direct inhibitory effects of taurine on norepinephrine-induced contraction in mesenteric artery of stroke-prone spontaneously hypertensive rats.
Li N, Sawamura M, Nara Y, Ikeda K, Yamori Y.
Graduate School of Human and Environmental Studies, Kyoto University, Japan.
The effect of taurine on vascular reactivity was investigated in the mesenteric artery of Wistar Kyoto (WKY), and stroke-prone spontaneously hypertensive rats (SHRSP). Administration of taurine significantly decreased blood pressure of SHRSP but not WKY. The mesenteric artery of taurine-treated SHRSP was excised to observe the contractile responses to transmural electrical stimulation and to several vasoactive substances. Vasocontraction induced by norepinephrine (NE) was significantly decreased by taurine. However, contraction elicited by the other substances tested was not affected. Consistently, when the vessels of SHRSP were pretreated with taurine in vitro, only the NE-induced vasocontraction was specifically attenuated. No effect was observed in WKY vessels. These results indicate that the hypotensive effect of taurine is accounted for at least in part its direct action on blood vessels.
PMID: 8915362 [PubMed - indexed for MEDLINE
Not entirely sure what to make of this next one. Anyone know anything about β3s deficient mice?
J Cardiovasc Pharmacol. 2003 Jan;41 Suppl 1:S127-31.
The effect of taurine on the salt-dependent blood pressure increase in the voltage-dependent calcium channel beta 3-subunit-deficient mouse.
Hagiwara K, Kuroki G, Yuan PX, Suzuki T, Murakami M, Hano T, Sasano H, Yanagisawa T.
Department of Molecular Pharmacology, Tohoku University School of Medicine, Sendai, Japan.
To examine the anti-hypertensive effect of taurine, we studied the effects of taurine on the salt-dependent blood pressure elevation, the electrocardiogram, and plasma catecholamine levels in the voltage-dependent calcium channel beta3-subunit-deficient mouse. In the wild-type mice, chronic high-salt loading (8% NaCl in chow) did not increase the blood pressure, whereas there was a significant increase in the systolic blood pressure in the beta3-subunit-deficient mice given a high-salt diet. Oral supplementation of taurine (3% in drinking water) could attenuate the increase in the blood pressure elicited by the high-salt diet. Plasma catecholamine levels were significantly decreased by the high-salt diet, and supplementation of taurine prevented those decreases in beta3-subunit-deficient mice. It is suggested, therefore, that chronic supplementation of taurine has an anti-hypertensive action in salt-dependent blood pressure elevation.
PMID: 12688409 [PubMed - indexed for MEDLINE
This one confirms that dietary sodium is a regulator of both central and peripheral NE metabolism:
Hypertension, Vol 3, 233-239, Copyright © 1981 by American Heart Association
Effect of chronic sodium depletion on cerebrospinal fluid and plasma catecholamines
KB Brosnihan, JE Szilagyi and CM Ferrario
To test the role of central neurogenic factors in sodium-depleted states, cerebrospinal fluid (CSF) norepinephrine, epinephrine, and dopamine were measured in mongrel dogs first on a normal sodium intake (65 mEq sodium/day) and then on a 21-day regime of low sodium diet (4 mEq/day combined with diuretics). Plasma catecholamines were measured in the same group of dogs. Three weeks of sodium depletion supplemented with diuretics caused a 24-fold increase in plasma renin activity, hemoconcentration, and elevated serum protein concentration. Both plasma and CSF sodium decreased significantly. After sodium depletion, plasma norepinephrine rose 76% but epinephrine and dopamine did not change. The same pattern was observed whether samples were obtained in conscious or anesthetized animals. In CSF, norepinephrine rose 44% during sodium depletion, while epinephrine and dopamine remained unchanged. The CSF norepinephrine was related inversely to the CSF sodium concentration and directly to plasma renin activity. These observations support the view that the combined procedure of restricted dietary sodium intake and diuretic therapy causes alterations in CSF norepinephrine in a direction compatible with possible overactivity of central noradrenergic neurons.
http://hyper.ahajour...bstract/3/2/233
And it's true in healthy humans as well:
Journal of Clinical Endocrinology & Metabolism Vol. 48, No. 1 26-31
doi:10.1210/jcem-48-1-26
Copyright © 1979 by the Endocrine Society.
Effect of Sodium Intake on Plasma Catecholamines in Normal Subjects
MARK S. ROMOFF, GERALD KEUSCH<a name="RFN2">, VITO M. CAMPESE, MAW-SONG WANG, ROBERT M. FRIEDLER, PETER WEIDMANN and SHAUL G. MASSRY Division of Nephrology and Department of Medicine, University of Southern California School of Medicine Los Angeles, California 90033
Address all correspondence and requests for reprints to: Shaul G. Massry, M. D., Professor of Medicine, Division of Nephrology, University of Southern California, School of Medicine, 2025 Zonal Avenue, Los Angeles, California 90033.
The effect of the state of sodium balance on the activity of the sympathetic nervous system has been evaluated previously by measuring urinary catecholamine excretion. Since urinary catecholamine may be affected by factors such as renal function or renal production of catecholamines, blood catecholamines may provide a better index of the activity of the sympathetic nervous system. The present study was undertaken to evaluate the effect of varying sodium intake on blood catecholamines.
Thirteen normal subjects were studied for a period of 3 weeks in a metabolic ward. They received during the first, second, and third week 10, 100, and 200 meq sodium/day, respectively. On the seventh day of each week, when the patients had achieved sodium balance, urinary sodium excretion as well as blood levels of PRA, norepinephrine (NE), epinephrine (Ep), and dopamine (D) were measured in the supine position, at 5, 10, 15, and 20 min of upright posture, and at the end of 40 min of ambulation. The results show that: 1) blood levels of NE, Ep, and D as well as PRA were significantly higher during low sodium intake than during medium or high sodium intake, 2) as in the case of PRA, there was an inverse relationship between the blood levels of NE, Ep, and urinary sodium excretion; 3) upright posture produced a significant increment in the blood levels of NE which was not affected by sodium intake; and 4) the increment in PRA with posture was significantly greater during low sodium intake than with medium high sodium intake.
The data demonstrate that: 1) the plasma levels of NE, Ep, and D are affected by the state of sodium balance, particularly during marked sodium depletion; and 2) meaningful interpretation of the significance of the blood levels of catecholamines should be made with reference to indices of sodium balance, such as urinary sodium excretion.
http://jcem.endojour...bstract/48/1/26
Magnesium can also help with psychological and vasoconstrictive sides of NE, but I think it's already been mentioned ITT.